Chapters

Part I: Antibiotic resistance - Local scenario

1.3 Vancomycin-resistant enterococci (VRE)

1. VRE were first reported in Europe in 1986. Since then, this resistant organism has spread throughout the world and has become a major nosocomial pathogen. Currently, Enterococcus faecium is the most important vancomycin-resistant species. In the United States and some European countries, VREfm has disseminated widely in the hospitals and old age homes (30).
2. In HK, the first case of VREfm was identified in 1997 in a patient returning from the United States. During 1997–2008, the occurrence of VRE was sporadic which on several occasions have led to small clusters (<5 to 10 cases) of nosocomial transmission. There had been no continued transmission in our healthcare system. In the mid-2000s, two ad hoc studies demonstrated that VRE was carried by <0.1% of patients in high risk areas (31–32).
3. In our public hospitals, a protracted outbreak of VREfm occurred since 2011. With the implementation of directly observed patient hand hygiene and other infection control measures, the outbreak was finally contained in 2015. In this outbreak, a total of 4,060 VREfm new cases were reported in local public hospitals from 2011–2015 (33).
4. Vancomycin resistance in enterococci is plasmid-mediated. The vanA gene is encoded in a transposon Tn1546 and vanB encoded in Tn1547. The transposons are mobile and able to disseminate the resistant gene to other more virulent organisms, e.g. Staphylococcus aureus. Therefore, despite the low pathogenicity of VRE, they can act as a reservoir of mobile resistance gene (34).
5. Hospital outbreaks caused by VRE have been increasingly reported worldwide. Molecular epidemiology study by multilocus sequence typing revealed that this rise is attributed to the spread of a genetic lineage of Enterococcus faecium clonal complex 17 (CC17), Table 1.6 (34–35). CC17 is currently the predominant clone seen in hospital outbreaks worldwide (36–40). The protracted outbreak of VREfm in HK’s public hospitals from 2011–2015 also involved strains that belonged to CC17 (33).
6. Most of the E. faecium CC17 isolates remained susceptible to linezolid. However in a Germany survey, selection of linezolid-resistance in epidemic-virulent CC17 strains occurred during linezolid therapy (36). It is due to the accumulation of mutations in position 2,576 of the 23S rRNA gene for at least one of the gene copies, necessary for acquisition of phenotypic linezolid resistance in E. faecium.
7. Molecular epidemiological study has shown that CC17 has been circulating in hospitals in the United States since early 1980s (34).

 

Table 1.6 Characteristics of vancomycin-resistant E. faecium CC17

Full version as PDF (3.90 MB)
Important Notices
Contact Us
How to cite IMPACT
Privacy Policy